Dynamic LVOT obstruction

Dynamic LVOT obstructin can occur due to several causes:
1. The most well-known cause is hypertrophic cardiomyopathy (HCM). The hypertrophied basal septal (the most common cause of HCM) causes narrowing of LVOT that is dependant on the preload and afterload. Sometimes the obstruction is not obvious and requires provocation with Valsalva's maneuver or vasodilators.
2. Narrowing of LVOT due to other causes (e.g.: subaortic membrane) can cause dynamic obstruction. So, with subaortic membrane part of the obstruction is fixed due to the presence of membrane itself. but sometimes there is a dynamic component due to the associated systolic anterior motion (SAM) of the anterior mitral leaflet. This is due to the Venturi effect, as increased velocity in the LVOT bulls the anterior mitral leaflet causing further narrowing of the LVOT.
3. With increased contractility of the basal portions of LV. This can occur in different situations. For example compensatory hypercontractility of the basal segments in cases of acute myocardial infarction involving the apical and mid segments. Another example is in case of stress cardiomypathy that typically involves the apical segments with the famous apical ballooning picture. The basal parts usually tries to compensate with increased contractility to keep the cardiac output unaffected. The third condition is increased contractility due to dminstration of dobutamine as during dobutamine stress echocardiographym, dynamic LVOT obstruction can occur and is one of the possible causes of hypotension that is worsened by the vasodilator effect of dobuamine. The presence of concentric LVH with small cavity is predisposing condition in all the three situation given here.
4. Cardiac amyloidosis should be suspected in dynamic LVOT obstruction. It can cause septal hypertrophy in association with reduced LV filling. Both togeather may lead to LVOT obstruction.
5. Mitral valve repair with ring: Here the anterior mitral leaflet is pushed rather than pulled into the LVOT in contrary to the other types of LVOT obstruction. Small LV cavity and long posterior leaflet predisposes to this situation.
6. Increased velocity in the LVOT with increase flow as in exercise, sepsis and severe anemias has been shown to cause LVOT obstruction in some cases. Here there is reduction of the afterload associated with tachycardia that causes reduced filling time and smalled LV cavity predisposing to dynamic LVOT obstruction.
7. Aortic valve replacement for treatment of aortic stenosis. Long standing aortic stenosis causes significant LVH. But as there is increased afterload due to the fixed obstruction at the valve level, this keeps the LV walls apart and no dynamic component is present. As the fixed obstruction is relieved with aortic valve replacement, the dynamic obstruction is unmasked. Dynamic obstruction here is more commen to happen at the midcavity level rather than LVOT.
8. Sigmoid septum in elderly patients can cause dynamic LVOT obstruction due to abnormal aortic angle but yet the exact mechanism is unclear.
9. In cases of L-TGA, the LVOT is open into the low pressure pulmonary circulation while the right ventricle is exposed to the systemic higher pressure circulation. This causes bulging of the interventricular septum to the left ventricle and subsequently may cause dynamic LVOT obstruction of a unique mechanism

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Assessment of the Left ventricular function in the presence of mitral regurge

The assessment of the rate of rise of LV pressure (dP/dt) can predict the intrinsic left vemtricular systolic function in a load-independent from. Thus it can be used in the assessment of left ventricular systolic function in the presence of mitral regurge. In fact, this method is under utilized in the daily practice.

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To take this measure you must have good picture of the maximum regurgitant jet. Then take a continuous wave doppler spectral profile with high sweep speed (100mm/sec or more). Then measure the time taken for the velocity to rise from 1m/sec to 3m/sec. From Bernolli equation: the pressure change in this time is 32mmHg (4(3)² – 4(1) ² = 36 – 4 = 32). Then dP/dt = 32/the measured time in seconds. Normally this value is > 1200. A dP/dt value from 800-1200 suggests mild systolic impairment. A dP/dt value <800>

LV systolic function	dP/dt	Time taken by LV to generate 32 mmHg
Normal	>1200	<27 br="" msec="">
Mild-moderate impairment	800 – 1200	27 – 40 msec
Sever impairment	<800 o:p="">

>40 msec

(click on the images to view full size)

The major advantage of this method is that it is independent from changes in the afterload as the measures are taken in the isovolumetric contraction phase (before the opening of the aortic valve. Also, this method is well-validated in comparison with cardiac catheterization results. Unfortunately this method is unreliable in cases of left ventricular dysynchrony as in cases of LBBB. Also, it is affected by left atrial compliance. So, it can not be used in cases of acute mitral regurge as the left atrial pressure is elevated and the left atrium is noncompliant. If the regurgitant jet is eccentric, excess care should be taken to make the cursor line at the direction of the jet and at its center to avoid false measurements. However sever aortic stenosis and systemic hypertension was found to affect the reliability of this method.

The dP/dt was found to have prognostic value in the course of chronic heart failure. It is also used to predict the postoperative left ventricular function before valve repair and replacement.

The same principle can be used in the assessment of the right ventricular systolic function with some modification. On the tricuspid valve the time is measured time interval is between the velocities 0 and 2 m/sec (due to the lower pressures on the right side). Thus the dP/dt value on the right side is calculated by dividing 16 on the time interval taken to raise the tricuspid regurge velocity from 0 to 2 m/sec. But this method is not well-validated to assess RV systolic function.

On the opposite side the –ve dP/dt, which is the rate of decline of left ventricular pressure, can be used as a measure for diastolic dysfunction.

References:

1- http://www.criticalecho.com/content/tutorial-5-assessment-lv-systolic-function

2- Feigenbaum's Echocardiography, 6th Edition

3- Echocardiography: the normal examination and echocardiographic measurements, by Bonita Anderson 2002.

4- The practice of clinical echocardiography, by Catherine M. Otto‏, 2007

5- Echocardiography Review Guide, by Catherine M. Otto and Rebecca Gibbons Schwaegler, 2007

6- Doppler-derived dP/dt and –dP/dt predict survival in congestive heart failure, Theodore J. Kolias, Keith D. Aaronson, and William F. Armstrong, 2000;36;1594-1599 J. Am. Coll. Cardiol.

7- A new method for estimating left ventricular dP/dt by continuous wave Doppler-echocardiography. Validation studies at cardiac catheterization, GS Bargiggia, C Bertucci, F Recusani, A Raisaro, S de Servi, LM Valdes-Cruz, DJ Sahn and L Tronconi, 1989;80;1287-1292 Circulation

Mitral valve . . . Where did this name come from?

Have you asked yourself this question. Why the left atrioventricular valve (or the bicuspid valve as some old books say) is commonly known as the mitral valve. In fact the name mitral is now the most commonly use name and it may sound strange somewhat if you use any either of the other 2 forementioned names. Then what does mitral mean. The word "mitre" is used to name the hat worn by catholic bishops and cardinals in ceremonies. Here is some mitre.

When you turn the open mitral valve upsidedown you will find it looking like the mitre. They say a picture worth 1000 word, so let us save the words. Here is the piture.